A human leukemic cell line has been used to study steroid actions. Spontaneous steroid resistant subclones have a unique defect in their glucocorticoid receptors. This r plus act 1 defect causes reduced numbers of receptors/cell with reduced capability for nuclear transfer. These receptors are labile under conditions for "activation." In HTC cells, mouse mammary tumor virus genes are being studied for possible correlations between methylation and lack of expression. Somatic cell hybrids between rat GH3 cells and mouse L cells contain both mouse and rat growth hormone (GH) genes which are not expressed. Re-expression of GH or prolactin (Prl) genes in segregating hybrids occurs independently. Several genomic clones for GH and Prl have been obtained. These clones have been mapped by restriction endonuclease and heteroduplex analyses. Novel potential affinity labels for glucocorticoid receptors have been synthesized and analyzed for apparent receptor affinity and biological activity. One is unique long-acting antiglucocorticoid. An unusual glucocorticoid is being studied for its antileukemic cell activity. A library of induced liver cDNA's is being prepared. A specific, saturable binding protein for oxygenated sterols has been characterized.